Dyspnea Emergensi FK - 2012 PDF

7/26/2019 Dyspnea Emergensi FK - 2012 PDF

1/86

dr Salim S Thalib


2/86

Respiration is controlled by areas of the brain

that stimulate the contraction of the diaphragm

and the intercostal muscles.

These areas, collectively calledRESPIRATORY CENTERS


3/86


4/86

Clustered neurons in the brain, located

bilaterally in the reticular formation of the brain

stem and from which nerve impulses are sent to

respiratory muscles.

Medullary Respiratory Centers

Pons Respiratory Centers


5/86

MEDULLARY RESPIRATORY CENTERS

Dorsal Respiratory Group

Inspiratory area


6/86

INSPIRATORY CENTER When fired they generates

rhythmic nerve impulses thattravel along the phrenic nerve

to diaphragm and intercostalnerves to excite externalintercostal muscles

As a result, these muscles willcontract and the thorax

expand, Volume increase

Pressure decrease

Air pushes into lungs


7/86


8/86

DRG then becomes dormant,

and expiration occurs passively

as the inspiratory muscle relax

and the lungs recoil.

This cyclic activity of the

inspiratory neurons repeats and

produce respiratory rate of 12

15 breaths per minute


9/86

MEDULLARY RESPIRATORY CENTERS

Ventral Respiratory Group

Expiratory area


10/86

VRG contain mix of neurons

Inspiratory

Expiratory (mainly)

Inactive during normal

respiration


11/86

Pontine respiratory group

A collection of neurons in the

reticular formation within the

pons

Transmit inhibitory impulses to

the inspiratory centers in

medulla


12/86

Factors influencing the respiratory center of the

brain

Pulmonary irritant reflexes

Receptors in the lung that respond to irritants

Activation of irritant receptors

Send signals to respiratory centers through vagal nerve

Modify respiratory rate and depth


13/86


brain

The inflation reflexes

Stretch Receptors (baroreceptors) in visceral

pleurae that stimulated when lung are inflated

Activation of stretch receptors

Send inhibitory signals to medullary respiratorycenters through vagus nerve

End inspiration and allow expiration


14/86


brain

Influence of higher brain centers

Hypothalamic controls

Activation of sympathetic centers in hypothalamus

Send signals to respiratory centers

Modify respiratory rate and depth


15/86


brain

Influence of higher brain centers

Cortical controls - voluntary controls

Cerebral motor cortex

Send signals to motor neurons

Stimulate respiratory muscles(Bypassing the medullary center)


16/86


brain

Chemical factors:

Oxygen (O2)

Carbon dioxide (CO2)

Hydrogen ion (H+)

Sensed by CHEMORECEPTORS


17/86


brain

CHEMORECEPTORS

Central chemoreceptors

Located in bilaterally in medulla

Sensitive to the pH ECF

Peripheral chemoreceptors Located in great vessels of neck

sensitive to PO2, PCO2and pH


18/86

Influence of PCO2 and H+

Most potent and

most closely

controlled

Sensed by central

chemoreceptors


19/86

Influence of PCO2 and H+


20/86

Cells sensitive to arterial

PO2are found in:

Peripheral

chemoreceptors:

Aortic bodies

In arch of aorta

Carotid bodies

In common carotid artery

Influence of PO2


21/86

Under normal condition the

decline in arterial PO2 has a

slight effect on ventilation.

Arterial PO2must decrease

to less than 60 mm Hg

before O2level becomemajor stimulus for increased

ventilation.

Influence of PO2


22/86

Influence of arterial pH

changes in arterial pH can

modify respiratory rate

and depth even when CO2

and O2are normal

Act on peripheralchemoreceptors.


23/86


24/86


25/86


26/86


27/86

INTRUDUCTION


28/86

DEFINITION OFDYSPNEA


29/86

MECHANISM OFDYSPNEA

DYSPNEA


30/86


31/86

RESEPTOR PADA SISTEM RESPIRASI


32/86


33/86


34/86

Kapasitas residu paru


35/86

obstruksi paru


36/86


37/86


38/86


39/86


40/86

Composed of four general categories

Pulmonary

Cardiac

Mixed cardiac or pulmonary

non-cardiac or non-pulmonary


41/86

Cardiac Etiology

CHF

CAD

MI (recent or past history)

Cardiomyopathy

Valvular dysfunction

Left ventricular hypertrophy

Pericarditis

Arrhythmias

Congestive heart failure

Coronary artery disease

Miocard infarct


42/86

COPD with pulmonary HTN and/or cor

pulmonale

Deconditioning

Chronic pulmonary emboli

Pleural effusion


43/86

Metabolic conditions (e.g. acidosis)

Pain

Trauma

Neuromuscular disorders

Functional (anxiety,panic disorders, hyperventilation)

Chemical exposure


44/86

VENTILASI

DIFUSIPERFUSI

Airway

Alveol

Kapiler darah


45/86


46/86

Pulmonary Etiology


47/86


48/86


49/86

No VENTILASI

PERFUSI

Airway

Alveol

Kapiler darah

Bood flow

S UNT UNIT

PERFUSION WITHOUT VENTIL TION

Sumbatan


50/86

SHUNT UNIT


51/86

Akibat alveoli yang kolaps, darah yang

mengaliri tidak mengalami oksigenasi

Perfus ion w i thout vent i lat ion shun t

(direct r igh t-to- lef t shunt)

Ratio ventilasi-perfusi terganggu

hipoksemia


52/86


53/86


54/86


55/86


56/86


57/86


58/86


59/86

AIR FLUID LEVEL


60/86


61/86


62/86


63/86


64/86


65/86


66/86


67/86


68/86


69/86


70/86


71/86


72/86

Barking cough, stridor, hoarseness

Difficul breathing worsen at night


73/86

Steeple sign


74/86


75/86


76/86


77/86


78/86


79/86


80/86


81/86


82/86


83/86

Pengisian alveoli oleh eksudat /cairan

Ventilasi berkurang / tidak ada

Unit shunt

Hipoksemia


84/86


85/86

Questions ?


86/86

Dyspnea Emergensi FK - 2012 PDF

Documents

Transcript of Dyspnea Emergensi FK - 2012 PDF